The Role of Norepinephrine and Estradiol in the Pathogenesis of Cardiac Wall Motion Abnormality Associated With Subarachnoid Hemorrhage

Abstract

Background and Purpose-The majority of patients with ventricular wall motion abnormality (WMA) associated with subarachnoid hemorrhage (SAH) are postmenopausal women. In addition to elevated catecholamine, the role of estrogen in the pathogenesis of WMA has recently been implicated. The objective of this study is to clarify the interrelation among catecholamine, estrogen, and WMA in patients with SAH. Methods-A retrospective analysis was performed on the medical records of 77 patients with SAH (23 men, 54 women) whose plasma levels of epinephrine, norepinephrine, and estradiol had been measured and echocardiograms had been obtained within 48 hours of SAH onset. Results-Twenty-four patients (31%) were found to sustain WMA on admission. Multivariate regression analysis revealed that decreased estradiol (Pϭ0.018; OR, 0.902) and elevated norepinephrine levels (Pϭ0.027; OR, 1.002) were associated with WMA. After quadrichotomization of 77 patients based on sex/WMA, plasma norepinephrine levels were markedly elevated in men with WMA, whereas estradiol levels were markedly decreased in women with WMA. Plasma norepinephrine and estradiol levels were not correlated. Fifty-four female patients with SAH were further quadrichotomized based on norepinephrine/estradiol levels with a threshold value of 1375 pg/mL for norepinephrine and 11 pg/mL for estradiol. The incidence of WMA in the high-norepinephrine/low-estradiol group was significantly higher than the low-norepinephrine/high-estradiol group. Conclusions-To our knowledge, this is the first study to evaluate the interrelation among catecholamine, estrogen, and SAH-induced WMA. Lack of estradiol in postmenopausal women may predispose them to develop WMA after poor-grade SAH. However, the precise role of multiple sex hormones in SAH-induced WMA should be evaluated in future prospective studies. (Stroke. 2012;43:1897-1903.)

Cardiac Troponin Elevation and Outcome after Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis

“…5,8,24,32,33 A more generally accepted hypothesis is that sympathetic stimulation induces catecholamine release in the myocardium, which may lead to impaired systolic and diastolic function, repolarization abnormalities, and myocardial damage. [2][3][4]34,35 Troponin is a highly specific and sensitive marker of cardiac injury. 7 The troponin complex is composed of 3 protein subunits, troponins T, I, and C. Troponins T and I exhibit unique cardiac isoforms, whereas cardiac and skeletal muscles share troponin C isoforms, rendering this protein unsuitable for diagnostic use.…”

Role of catecholamines in acute hypertensive response

“…Among several proposed mechanisms of the acute hypertensive reaction, the massive release of catecholamines into the systemic circulation has been considered pivotal both in SAH and in SICH patients [1][2][3][4][5][6]. However, the relationship between admission SBPs and plasma catecholamine levels in each hemorrhagic stroke subtype has rarely been studied.…”

“…It is frequently observed in patients with hemorrhagic stroke -that is, subarachnoid hemorrhage (SAH) and spontaneous intracerebral hemorrhage (SICH), many of whom have chronic hypertension [4]. Among several pathomechanisms of the acute hypertensive response in hemorrhagic stroke patients, activation of the sympathetic nervous system, exemplified by elevated plasma catecholamine levels, may play a pivotal role [5,6]. However, few studies have evaluated the relationship between admission SBPs and plasma catecholamine levels in hemorrhagic stroke patients: it is possible that the acute hypertensive response in SAH and SICH patients may not be identical [6], and if this is the case, BPs in SAH and SICH patients may have to be managed differently.…”

The Serum Level of Brain Natriuretic Peptide Increases in Severe Subarachnoid Hemorrhage thereby Reflecting an Increase in Both Cardiac Preload and Afterload

“…A previous study clarified that excessive catecholamine secretion provided the ventricular wall motion abnormality [31,32] and cardiomyopathy [21,22] in severe SAH patients. We can predict that the rapid elevation of serum catecholamine may induce the neurogenic cardiomyopathy itself reflected by the increase of sBNP and the cardiac preload (i.e., increase of GEDI and ITVI in our results) in severe SAH patients.…”